Leung Yiu Fai Ivan. / "July 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 83-101). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Chan Shun Wan. / "August 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 217-235). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Conclusions. SBL showed its efficacy in treating the animal model of allergic rhinitis. Its mechanisms may be related to its suppressive action on PCA reaction, the production of TXB2 and the expression of eNOS, as well as its modulation of cytokines, including IL-4, IL-6, IL-8, GM-CSF and TNF-alpha, release from mast cells. The clinical trial showed that SBL had more beneficial action on the quality of life, in comparison to the placebo, in the domains of RE and BP. Some symptoms evaluations of PAR patients, including GF, NB and SF were more markedly improved in the SBL group when compared with the placebo group. Furthermore, the use of SBL, with the study dose and treatment period, was safe. However, the accurate efficacy and mechanisms of SBL are largely unknown and need further investigation. (Abstract shortened by UMI.) / Introduction. Although great progress in treatment of allergic rhinitis have made in recent years, remarkably increasing prevalence and cost in epidemiology studies strongly suggest the difficulties in the management of allergic rhinitis. Shi-Bi-Lin (SBL) is a formula modified from the traditional Chinese herbal formula Cang-Er-Zi-San (CEZS) and a classic European formula SinupretRTM. CEZS has been used for the treatment of allergic rhinitis for several centuries in East Asia communities, and SinupretRTM has been used in treating paranasal sinusitis and rhinitis widely in Europe for decades. However, its therapeutic mechanisms remain unclear. We examined the efficacy and the possible mechanism of SBL in an animal model of allergic rhinitis and in cell culture study using Human Mast Cell Line (HMC-1) and Peripheral Blood Mononuclear Cells (PBMC). In addition, a clinical trial was conducted to examine its clinical efficacy and safety. / Results. In the animal study, SBL showed a potent effect in relieving the symptoms of nasal obstruction, sneezing and nasal scratching (P<0.05 or P<0.01), but had no convincing effect in decreasing the nasal discharge (P>0.05). In PCA test, IgG1 increased in a modest manner in the SBL-treated group when compared with the sham group (P<0.05 or P<0.01). Eosinophil infiltration and the expression of eNOS in nasal mucosa, but not iNOS, were obviously lower in the SBL treated group (P<0.05 or P<0.01) in comparison to the sham group. The levels of thromboxane B (TXB)2 in the nasal lavage fluid, but not histamine and peptide leukotrienes (p-LTs), showed significantly lower than that of the sham group (P<0.05). In vitro study showed that SBL modulated the cytokines, including interleukin (IL)-4, IL-6, IL-8, Granulocyte/Macrophage Colony-Stimulating Factor (GM-CSF) and tumor necrosis factor (TNF)-alpha, release from human mast cell line (HMC-1). However, the mRNA expressions of these cytokines were not significantly altered. As the controls, dexamethasone, desloratadine and budesonide had more potently inhibitory effects on cytokines release from HMC-1. The component herbs generally had stimulatory effects on the cytokine release from HMC-1 and variable effects on PBMC. In the clinical trial, a total of 84 patients were recruited in the clinical trial and 77 of them completed the trial. Although no significant differences of each domain between the SBL and placebo groups were detected, findings supported the efficacy of SBL were obtained. / by Zhao Yu. / "July 2005." / Advisers: C. A. Van Hasselt; Ping-Chung Leung; Kong-Sang Woo. / Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0172. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.

by Fung Yin Lee, Annie. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 181-189). / ABSTRACT --- p.i / LIST OF ABBREVIATIONS --- p.iv / ACKNOWLEDGEMENT --- p.v / TABLE OF CONTENTS --- p.vi / LIST OF FIGURES --- p.ix / INTRODUCTION --- p.1 / LITERATURE REVIEW --- p.4 / Chapter I. --- A. Arterial pressure --- p.4 / Chapter B. --- Regulation of arterial pressure --- p.7 / Chapter II. --- Hypertension --- p.14 / Chapter III. --- Treatment of hypertension --- p.29 / Chapter IV. --- Plants and their effects on blood pressure --- p.48 / Chapter V. --- Characteristics of the three plants being studied --- p.50 / MATERIALS AND METHODS --- p.55 / Chapter A. --- Preparative procedures --- p.55 / Chapter 1. --- Preparation of plant extracts --- p.55 / Chapter 2. --- Animal preparation for invivo blood pressure measurement --- p.56 / Chapter 3. --- Preparation of right atria for in vitro studies --- p.56 / Chapter 4. --- Preparation of artery strips for in vitro studies --- p.57 / Chapter 5. --- Preparation for diuretic studies --- p.58 / Chapter B. --- Experiments done --- p.60 / Chapter 1. --- Cumulative dose response of individual plant extract --- p.60 / Chapter 2. --- Combination of plant extracts --- p.60 / Chapter 3. --- Pharmacological antagonists studies --- p.64 / Chapter a. --- Autonomic ganglion transmission --- p.64 / Chapter b. --- Alpha adrenergic activity --- p.64 / Chapter c. --- Beta adrenergic activity --- p.65 / Chapter d. --- Cholinergic activity --- p.65 / Chapter e. --- Histaminergic activity --- p.65 / Chapter f. --- Serotoninergic activity --- p.65 / Chapter 4. --- Urinary and sodium excretionin water loaded rats --- p.66 / Chapter 5. --- Studies on chronotropic and inotropic effects on isolated right atrium --- p.66 / Chapter a. --- Effect of individual plant extract --- p.66 / Chapter b. --- Effect of combination of plant extracts --- p.66 / Chapter 6. --- Effect of plant extract on contractile responses of rat tail artery strips --- p.70 / Chapter a. --- Effect of individual plant extract --- p.70 / Chapter b. --- Effect of combination of plant extracts --- p.70 / Chapter 7. --- Effect of acute oral feeding of plant extracts on blood pressure of rats --- p.71 / Chapter C. --- Statistics --- p.71 / RESULTS / Chapter A. --- Preparation of plant extracts --- p.72 / Chapter B. --- Effect of plant extracts on blood pressure changes --- p.72 / Chapter 1. --- Individual plant extract --- p.72 / Chapter 2. --- Combination of two plant extracts --- p.73 / Chapter 3. --- Combination of three plant extracts --- p.76 / Chapter C. --- Pharmacological antagonist studies --- p.79 / Chapter 1. --- Autonomic ganglion transmission --- p.79 / Chapter 2. --- Alpha adrenergic activity --- p.79 / Chapter 3. --- Beta adrenergic activity --- p.81 / Chapter 4. --- Cholinergic activity --- p.82 / Chapter 5. --- Histaminergic activity --- p.83 / Chapter 6. --- Serotoninergic activity --- p.84 / Chapter D. --- Urinary and sodium excretion in water loaded rats --- p.85 / Chapter E. --- Chronotropic and inotropic studies of isolated right atrium --- p.88 / Chapter 1. --- Effect of individual plant extract --- p.88 / Chapter 2. --- Effect of combination of plant extracts --- p.89 / Chapter F. --- Effect of plant extracts on contractile responses of rat tail artery strips --- p.101 / Chapter G. --- Effect of acute oral feeding of plant extracts on MAP of rats --- p.102 / DISCUSSION --- p.156 / Chapter A. --- Comment on preparation of plant extracts --- p.156 / Chapter B. --- The hypotensive effects of the plant extracts --- p.157 / Chapter C. --- The mechanism of action --- p.159 / Chapter D. --- The renal effect of plant extracts --- p.161 / Chapter E. --- The interaction of the hypotensive effect of plant extracts --- p.164 / Chapter F. --- In vitro studies --- p.167 / Chapter G. --- The oral effect of the plant extracts --- p.174 / SUMMARY --- p.176 / CONCLUSION --- p.179 / REFERENCES --- p.181 / APPENDIX --- p.190 / "Appendix I To study the hypotensive effects of trypsin treated green bean, rue and kelp" --- p.191 / "Appendix II To study the hypotensive effects of ether treated green bean, rue and kelp" --- p.194

Leung Lai-Kin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 110-113). / Abstracts in English and Chinese. / Abstract English --- p.i / Chinese --- p.iii / Acknowledgments --- p.v / Table of contents --- p.vi / List of Tables --- p.ix / List of Figures --- p.x / List of Abbreviations --- p.xiii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter Chapter 2 --- Establishment of compound formulation --- p.4 / Chapter 2.1 --- Formulation research --- p.4 / Chapter 2.2 --- Aqueous extract preparation --- p.6 / Chapter 2.2.1 --- Materials and Methods --- p.6 / Chapter 2.2.2 --- Results --- p.7 / Chapter 2.2.3 --- Discussion --- p.9 / Chapter 2.3 --- Preliminary test --- p.10 / Chapter 2.3.1 --- Materials and Methods --- p.10 / Chapter 2.3.2 --- Results --- p.12 / Chapter 2.3.3 --- Discussion --- p.14 / Chapter Chapter 3 --- Quality Control --- p.15 / Chapter 3.1 --- HPLC standardization --- p.16 / Chapter 3.2 --- Materials and Methods --- p.19 / Chapter 3.3 --- Results --- p.20 / Chapter 3.4 --- Discussion --- p.28 / Chapter Chapter 4 --- Antioxidant study --- p.29 / Chapter 4.1 --- Red blood cell hemolysis model --- p.30 / Chapter 4.1.1 --- Materials and Methods --- p.30 / Chapter 4.1.2 --- Results --- p.30 / Chapter 4.1.3 --- Discussion --- p.32 / Chapter 4.2 --- Ischemia-Reperfusion on Langendorff --- p.33 / Chapter 4.2.1 --- Materials and Methods --- p.34 / Chapter 4.2.2 --- Results --- p.37 / Chapter 4.2.3 --- Discussion --- p.60 / Chapter Chapter 5 --- Vasodilation study --- p.61 / Chapter 5.1 --- Vasodilation in organ bath --- p.63 / Chapter 5.1.1 --- Materials and Methods --- p.63 / Chapter 5.1.2 --- Results --- p.65 / Chapter 5.1.3 --- Discussion --- p.79 / Chapter 5.2 --- Endothelium dependent vasodilation --- p.80 / Chapter 5.2.1 --- Materials and Methods --- p.80 / Chapter 5.2.2 --- Results --- p.83 / Chapter 5.2.3 --- Discussion --- p.95 / Chapter Chapter 6 --- Anti-platelet study --- p.96 / Chapter 6.1 --- CFU-MK plasma clot colony assay --- p.97 / Chapter 6.2 --- Materials and Methods --- p.97 / Chapter 6.3 --- Results --- p.100 / Chapter 6.4 --- Discussion --- p.103 / Chapter Chapter 7 --- Discussions and prospects --- p.104 / Chapter 7.1 --- Discussions --- p.104 / Chapter 7.2 --- Prospects --- p.107 / Chapter 7.2.1 --- TCM capsule with GMP --- p.107 / Chapter 7.2.2 --- Clinical Trial of the capsule --- p.109 / References --- p.110

丹參和葛根為我國民間常用的傳統藥材, 常用於心血管疾病的治療。本試驗主要研究丹參葛根複方(DG, 7:3)對大鼠基底動脈的舒張作用 及腦保護作用。 / 上述所有藥物對U46619預收縮的基底動脈環呈現濃度依賴性的舒張作用。一氧化氮合酶抑制劑L-NAME以及鳥苷酸環化酶抑制劑ODG部分抑制葛根素的舒張作用。在另一組去內皮試驗中, 腺苷酸環化酶抑制劑SQ22536, 鳥苷酸環化酶抑制劑ODG, 大電導鈣離子依賴型鉀通道抑制劑Iberiotoxin以及電壓門控型鉀通道抑制劑4-AP對所有藥物的舒張作用沒有影響。然而， ATP型鉀通道抑制劑格列本脲能夠抑制丹參葛根複方，丹參，葛根，丹參素，葛根素，大豆苷以及大豆苷元的最大舒張反應。內向整流型鉀通道抑制劑氯化鋇則降低丹參酚酸B和大豆苷元的最大反應值。非選擇性鉀通道抑制劑乙基氯化銨以及所有鉀通道抑制劑的混合物顯著抑制上述所有藥物的舒張作用。除了葛根素之外，所有的藥物動度依賴性的抑制氯化鈣所引起的血管收縮。 / 體內研究發現大鼠經歷10分鐘雙側頸總動脈夾閉合並低血壓，及24小時的複灌後，與假手術組動物相比，腦血流量顯著降低，氧化性損傷明顯可見。連續7天口服丹參葛根複方（0.3g/kg 和 3g/kg）, 丹參 (3g/kg)，或者葛根 (3g/kg)對血壓沒有影響。但是，高劑量的丹參葛根複方 (3g/kg) 能夠提高超氧化物歧化酶和過氧化氫酶的活性，抑制丙二醛和一氧化氮的產生。3g/kg的葛根可以提高超氧化物歧化酶的活性，3g/kg的丹參則能抑制一氧化氮的產生。在大鼠中動脈阻塞模型中，連續7天口服丹參葛根複方（3g/kg）能明顯降低腦部的梗死率，同時改善大鼠的神經行為學。 / 總體來說，研究發現丹參葛根複方，丹參，葛根，丹參酚酸B，大豆苷以及大豆苷元的血管舒張作用是通過開平滑肌細胞的通鉀離子通道以及抑制鈣離子內流而實現的。然而葛根素的血管舒張作用是內皮依賴性的，通過產生一氧化氮，開放平滑肌細胞的鉀離子通道而實現的。丹參葛根複方能起到一定的腦保護作用。總而言之，研究表明上述藥物可能會對阻塞性腦血管病的人群有益處。 / Danshen and gegen are used in traditional Chinese medicine for the treatment of cardiovascular diseases. In this study, the relaxant actions of a danshen and gegen formulation (DG; ratio 7:3) and its constituents were investigated on rat-isolated cerebral basilar artery. In addition, the neuroprotective effect of DG was explored in rats subjected to global and focal ischaemia. / DG and all its constituents produced concentration-dependent relaxation of the artery rings precontracted by U46619. Removal of the endothelium had no effect on their vasodilator actions except the maximum response (I[subscript max]) to puerarin was inhibited by 42%. The nitric oxide synthase (NOS) inhibitor L-NAME and guanylyl cyclase (GC) inhibitor ODQ but not the cyclo-oxygenase (COX) inhibitor flurbiprofen produced partial inhibition on the puerarin-induced effect. In a set of endothelium-denuded artery rings, adenylyl cyclase (AC) inhibitor SQ22536, GC inhibitor ODQ, KV channel inhibitor 4-aminopyridine (4-AP) and BK[subscript Ca) channel inhibitor iberiotoxin had no influence on their vasodilator actions. However, pretreatment with K[subscript ATP] channel inhibitor glibenclamide reduced Imax to DG, danshen, gegen, danshensu, puerarin, daidzein and daidzin. K[subscript IR] inhibitor barium chloride (BaCl₂) reduced II[subscript max] to salvianolic acid B and daidzein. The non-selective K⁺ channel inhibitor tetraethylammonium (TEA), or a combination of all the K⁺ channel inhibitors produced significant partial inhibitions on all the agents’ actions. Electrophysiological studies on smooth muscle cells isolated from rat basilar artery also confirmed that DG, danshen, gegen danshensu, puerarin, daidzein and daidzin elevated K[subscript ATP] currents. In addition, DG and all its constituents, except puerarin, produced concentration-dependent inhibition on CaCl₂-induced vasoconstrictions. These findings were confirmed by con-focal microscopy studies. / In vivo study on a rat model of global ischaemia showed that challenging the rats with 10 min bilateral common carotid artery occlusion combined with hypotension, and followed by 24 h reperfusion produced significant decrease in cerebral blood flow and oxidative damage compared to sham-operated animals. Administration of DG (0.3 g/kg and 3 g/kg, p.o.), danshen (3 g/kg, p.o.) or gegen (3 g/kg, p.o.) for 7 days had no effect on blood pressure. However, the 7 days treatment with DG (3 g/kg) restored superoxide dismutase (SOD) and catalase (CAT) activities, suppressed the production of maleic dialdehyde (MDA), and inhibited the production of nitric oxide (NO). In addition, gegen (3 g/kg) restored SOD enzyme activity, whereas, danshen (3 g/kg) inhibited NO production. In addition, treatment with DG (3 g/kg) showed a significant reduction in infarct weight and improved the neurological deficit in a rat model of focal cerebral ischaemia induced by middle cerebral artery occlusion (MCAO). / In conclusion, the vasorelaxant actions of DG, danshen, gegen, salvianolic acid B, danshensu, daidzein and daidzin were found to involve the opening of K⁺ channels and inhibition of Ca²⁺ influx in the vascular smooth muscle cells. In contrast, puerarin produced vasodilatation via an endothelium-dependent mechanism involving NO production and an endothelium-independent pathway mediated by the opening of K⁺ channels. DG may have some cerebro-protective effects. Overall, the present studies showed that DG and its constituents could be beneficial to patients with obstructive cerebrovascular diseases. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Deng, Yan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 164-178). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / ABSTRACT --- p.v / 摘要 --- p.iviii / ACKNOWLEDGEMENTS --- p.x / PUBLICATIONS BASED ON THIS THESIS --- p.xii / ABBREVIATIONS --- p.xiv / Chapter CHAPTER 1 --- Introduction --- p.1 / Chapter 1.1 --- Chinese Medicines in treatment of cerebrovascular diseases --- p.2 / Chapter 1.2 --- Danshen --- p.4 / Chapter 1.2.1 --- Chemical constituents --- p.4 / Chapter 1.2.1.1 --- Hydrophilic compounds of danshen --- p.4 / Chapter 1.2.1.2 --- Lipophilic compounds of danshen --- p.5 / Chapter 1.2.1.3 --- Other compounds --- p.5 / Chapter 1.2.2 --- Pharmacological activities --- p.5 / Chapter 1.2.2.1 --- Vascular protection --- p.5 / Chapter 1.2.2.2 --- Anti-tumour --- p.7 / Chapter 1.2.2.3 --- Treatment of liver diseases --- p.8 / Chapter 1.2.2.4 --- Treatment of drug addiction --- p.9 / Chapter 1.2.2.5 --- Treatment of kidney diseases --- p.10 / Chapter 1.2.3 --- Pharmacokinetics --- p.10 / Chapter 1.3 --- Gegen --- p.12 / Chapter 1.3.1 --- Chemical constituents --- p.12 / Chapter 1.3.2 --- Pharmacology --- p.13 / Chapter 1.3.2.1 --- Vascular effects --- p.13 / Chapter 1.3.2.2 --- Anti-diabetes --- p.14 / Chapter 1.3.2.3 --- Anti-hypercholesterolaemia --- p.15 / Chapter 1.3.2.4 --- Anti-inflammation --- p.16 / Chapter 1.3.2.5 --- Anti-platelet aggregation --- p.17 / Chapter 1.3.3 --- Pharmacokinetics --- p.17 / Chapter 1.4 --- Danshen and gegen formulation --- p.19 / Chapter 1.5 --- Mechanisms of vasodilatation --- p.22 / Chapter 1.5.1 --- Endothelium derived relaxant factors (EDRFs) --- p.22 / Chapter 1.5.1.1 --- Nitric oxide (NO) --- p.22 / Chapter 1.5.1.2 --- Prostacyclin (PGI₂) --- p.23 / Chapter 1.5.1.3 --- Endothelium-derived hyperpolarizating factors (EDHFs)- --- p.23 / Chapter 1.5.2 --- Signal transduction pathways --- p.24 / Chapter 1.5.2.1 --- Guanylyl cyclase-cGMP pathway --- p.24 / Chapter 1.5.2.2 --- Adenylyl cyclase-cAMP pathway --- p.24 / Chapter 1.5.3 --- Ion channels --- p.25 / Chapter 1.5.3.1 --- Potassium channels (K⁺ channels) --- p.25 / Chapter 1.5.3.2 --- Calcium channel (Ca²⁺ channels) --- p.25 / Chapter 1.6 --- Aims of study --- p.27 / Chapter CHAPTER 2 --- Materials and method --- p.28 / Chapter 2.1 --- Herbal preparation --- p.28 / Chapter 2.1.1 --- DG, danshen and gegen preparation --- p.28 / Chapter 2.1.2 --- Identification and quantification of chemical markers in DG water extract --- p.29 / Chapter 2.2 --- Experiments on rat basilar artery --- p.30 / Chapter 2.2.1 --- Animals --- p.30 / Chapter 2.2.2 --- Chemicals --- p.30 / Chapter 2.2.3 --- Isolation and mounting of blood vessels --- p.33 / Chapter 2.2.4 --- Protocols --- p.34 / Chapter 2.2.4.1 --- Effects on U46619-precontracted tone --- p.34 / Chapter 2.2.4.2 --- Endothelium-dependent mechanism --- p.34 / Chapter 2.2.4.3 --- Endothelium-independent mechanism --- p.35 / Chapter 2.2.4.4 --- Calcium channels --- p.36 / Chapter 2.2.4.5 --- Positive control --- p.36 / Chapter 2.2.5 --- Statistical analysis --- p.37 / Chapter 2.3 --- Experiments on rat cerebral basilar artery smooth muscle cells K[subscript ATP] channals --- p.38 / Chapter 2.3.1 --- Animals --- p.38 / Chapter 2.3.2 --- Chemicals --- p.38 / Chapter 2.3.3 --- Isolation of rat cerebral vascular smooth muscle cells --- p.40 / Chapter 2.3.4 --- Whole cell patch-clamp electrophysiology --- p.40 / Chapter 2.3.5 --- Statistical analysis --- p.44 / Chapter 2.4 --- Experiments on rat cerebral basilar artery smooth muscle cells calcium channels --- p.45 / Chapter 2.4.1 --- Animals --- p.45 / Chapter 2.4.2 --- Chemicals --- p.45 / Chapter 2.4.3 --- Isolation of rat cerebral vascular smooth muscle cells --- p.47 / Chapter 2.4.4 --- Dye loading and determination of [Ca²⁺]i --- p.47 / Chapter 2.4.5 --- Statistical analysis --- p.48 / Chapter 2.5 --- In vivo study of global ischaemia --- p.49 / Chapter 2.5.1 --- Animals --- p.49 / Chapter 2.5.2 --- Drugs and chemicals --- p.49 / Chapter 2.5.3 --- Experimental protocols for global ischaemia --- p.49 / Chapter 2.5.4 --- Induction of global ischaemia --- p.50 / Chapter 2.5.5 --- Blood pressure measurement --- p.52 / Chapter 2.5.6 --- Measurement of cerebral blood flow --- p.52 / Chapter 2.5.7 --- Biochemical assessment --- p.53 / Chapter 2.5.7.1. --- Dissection and homogenization --- p.53 / Chapter 2.5.7.2. --- Measurement of malondialdehyde (MDA) --- p.53 / Chapter 2.5.7.3. --- Estimation of nitrite --- p.53 / Chapter 2.5.7.4 --- Superoxide dismutase activity (SOD) --- p.54 / Chapter 2.5.7.5 --- Reduced glutathione (GSH) --- p.54 / Chapter 2.5.7.6 --- Catalase (CAT) --- p.55 / Chapter 2.5.7.7 --- NOS activity --- p.55 / Chapter 2.5.7.8 --- Protein --- p.56 / Chapter 2.5.8 --- Statistical analysis --- p.56 / Chapter 2.6 --- In vivo study of focal ischaemia --- p.57 / Chapter 2.6.1 --- Animals --- p.57 / Chapter 2.6.2 --- Drugs and chemicals --- p.57 / Chapter 2.6.3 --- Experimental protocols for global ischaemia --- p.57 / Chapter 2.6.4 --- Focal cerebral ischaemia-reperfusion model --- p.57 / Chapter 2.6.5 --- Assessment of neurobehavioural changes --- p.59 / Chapter 2.6.6 --- Assessment of cerebral infarction --- p.60 / Chapter 2.6.7 --- Statistical analysis --- p.60 / Chapter CHAPTER 3 --- Results --- p.61 / Chapter 3.1 --- Identification and quantification of chemical markers in DG water extract --- p.61 / Chapter 3.2 --- Effects of DG and its constituents on rat cerebral basilar artery --- p.64 / Chapter 3.2.1 --- Investigations on endothelium-dependent mechanisms --- p.64 / Chapter 3.2.2 --- Investigations on endothelium-independent mechanisms --- p.68 / Chapter 3.2.3 --- Positive control --- p.86 / Chapter 3.2.3 --- Investigations on calcium channels --- p.88 / Chapter 3.3 --- Effects of DG and its constituents on rat cerebral basilar artery smooth muscle cells --- p.91 / Chapter 3.3.1 --- Effects of water crude-extracts of DG, danshen, and gegen on K[subscript ATP] channels --- p.91 / Chapter 3.3.2 --- Effects of active constituents of danshen hydrophilic fraction on K[subscript ATP] channels --- p.100 / Chapter 3.3.3 --- Effects of the major isoflavonoids of gegen on K[subscript ATP] channels --- p.105 / Chapter 3.4 --- Effects of DG and its constituents on calcium channels of basilar artery smooth muscle cells --- p.112 / Chapter 3.5 --- Effects of DG, danshen and gegen on rat global ischaemia --- p.117 / Chapter 3.5.1 --- Effects of DG, danshen and gegen on rats’ blood pressure and cerebral blood flow --- p.117 / Chapter 3.5.2 --- Effects of DG, danshen and gegen on lipid peroxidation --- p.120 / Chapter 3.5.3 --- Effects of DG, danshen and gegen on SOD activity --- p.120 / Chapter 3.5.4 --- Effects of DG, danshen and gegen on CAT activity --- p.120 / Chapter 3.5.5 --- Effects of DG, danshen and gegen on reduced GSH level --- p.121 / Chapter 3.5.6 --- Effects of DG, danshen and gegen on NOS system --- p.126 / Chapter 3.6 --- Effect of DG on rat focal ischaemia --- p.129 / Chapter 3.6.1 --- Effect of DG on cerebral infarction --- p.129 / Chapter 3.6.2 --- Effect of DG on neurological deficits --- p.129 / Chapter CHAPTER 4 --- Discussion --- p.132 / Chapter 4.1 --- Studies of DG and its constituents on rat cerebral basilar artery --- p.133 / Chapter 4.1.1 --- Constituents of DG on U46619-precontracted tone --- p.133 / Chapter 4.1.2 --- Investigations on endothelium-dependent mechanisms --- p.133 / Chapter 4.1.3 --- Investigations on endothelium-independent mechanisms --- p.136 / Chapter 4.1.4 --- Investigations on calcium channels --- p.139 / Chapter 4.2 --- Effects of DG and its constituents on rat cerebral basilar artery smooth muscle cell K[subscript ATP] channels --- p.143 / Chapter 4.3 --- Effects of DG and its constituents on calcium influx in rat basilar artery smooth muscle cells --- p.147 / Chapter 4.4 --- Effects of DG, danshen and gegen on rat transient global ischaemia --- p.150 / Chapter 4.4.1 --- Effects of DG, danshen and gegen on rats’ blood pressure and cerebral blood flow --- p.150 / Chapter 4.4.2 --- Effects of DG, danshen and gegen on lipid peroxidation, SOD and CAT activity, and GSH level --- p.152 / Chapter 4.4.3 --- Effects of DG, danshen and gegen on NOS system --- p.155 / Chapter 4.5 --- Effects of DG on rat focal ischaemia --- p.157 / Chapter 4.6 --- Further studies --- p.160 / Chapter 4.7 --- Conclusion --- p.162 / REFERENCES --- p.164

Angiogenesis is a process of new blood vessels sprouting from the pre-existing vasculature, and mediated by multiple angiogenic and anti-angiogenic factors. Disturbance of the balance often leads to development of neovascular diseases. Neovascularization affecting the eye is a common cause of visual impairment and even blindness, particularly when corneal or choroidal neovascularization (NV) is involved. While there are effective treatment modes for ocular neovascularization, they are expensive and only inhibit disease progress. Since herbal medicine has been applied for anti-angiogenesis and anti-carcinogenesis therapies, we investigate the anti-angiogenic effect of selected herbal molecules: isoliquiritigenin (ISL), a flavonoid from licorice; epigallocatechin gallate (EGCG), a polyphenol from green tea; and resveratrol (Rst), a polyphenol phytoalexin derived from grapes. / In conclusion, by in vitro and in vivo studies, we showed that ISL, EGCG and Rst contributed to anti-angiogenesis via different biological mechanisms. We propose that these three herbal molecules (ISL, EGCG and Rst) are candidate anti-angiogenic agents for the treatment of ocular angiogenesis diseases. Their distribution profiles and pharmacokinetic properties should be investigated. / Results showed that sub-toxic levels of ISL (10 microM), EGCG (50 microM) and Rst (10microM) effectively suppressed endothelial cell proliferation and migration in the scratch-wound assay. Treatment with ISL was found to significantly up-regulate PEDF, which is known as a potent angiostatic factor. EGCG and Rst downregulate VEGF signaling cascade by suppressing Akt and FAK activation and affecting MMP-2, MMP-9 expression. In vivo angiogenesis assays further showed the suppressive effect of ISL, EGCG and Rst on neovascularization in three different animal models. Application of ISL at 1 microM showed the suppressive effect on chick CAM assay, corneal NV and choroidal NV assays consistently, the most effective dosage was close to 10 microM. EGCG at 1 microM showed the effect to reduce chick CAM vessel formation and corneal NV, and at 10 microM (the lowest tested concentration) to suppress choroidal NV in mice. Variable effects were observed in Rst treatment. Rst at 10 microM prohibited vessel growth in chick CAM, and 1 microM suppressed corneal NV formation and 2 microM deterred choroidal NV development. / This thesis contains two major parts. The first in vitro cell-based analysis investigated the toxicity of these herbal chemicals and their effect on endothelial cell growth and migration. The expression profile of vascular endothelial growth factor (VEGF) signaling cascade events, including Akt and focal adhesion kinase (FAK) activation, VEGF, pigment epithelium-derived factor (PEDF) and matrix metalloproteinases (MMPs) were examined by Western blotting. Then three in vivo models were established to study the effect of these herbal chemicals on angiogenesis. They were (1) developmental angiogenesis in chick chorioallantoic membrane (CAM), (2) pathological angiogenesis in silver nitrate cauterization-induced corneal neovascularization in BALB/c mice and, (3) laser photocoagulation-induced choroidal neovascularization in C57BL/6 mice. Changes of vascularization were determined by qualification of vessel number changes on the edge of gelatin sponge in 24 hours (chick CAM assay), measurement of vascularized area, live imaging of vessel leakage (fundus fluorescence angiography, FFA) and immunochemistry using antibodies specific for endothelial cells (corneal & choroidal NV assays) respectively. / Liu, Huanming. / Adviser: Chi Pui Pang. / Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 155-180). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

黑色素生成是為了保護皮膚細胞免受紫外光傷害的一個生化過程。在這過程中，黑色素在人類表皮底層的黑色素細胞的黑色素體內產生。該過程可以被基因，荷爾蒙或環境因素所影響。黑色素的製造量是依賴速度限制酶酪氨酸酶的活性，黑色素體的數量和大小，黑色素體通過黑色素細胞的偽足傳送致角質細胞的速度及黑色素體在角質細胞內的分佈。這些細胞過程會受皮膚顏色或紫外光曝光量的變化而影響。當黑色素的產生超過黑色素的降解，黑色素沉著毛病便出現。根據不同的皮膚類型，年齡組別及累積紫外光曝光程度而引發雀斑或黃褐斑的形成。很多治療方法市面上能夠提供，它們包括人工合成化粧品，激光，整容手術等。這些治療方法通常會產生副作用及蘊藏高風險。因此從天然物質裏尋找治療藥物便成了美容學的一個新的研究方向。在這研究裏，十種草本植物就從自古以來用作治療黑色素沉著毛病的傅統中藥中被挑選出來。那些草本植物被四種擁有不同極性的溶劑提取。小鼠黑色素細胞被用以篩選提取物的降黑色素能力。結果發現當歸的正己烷及二氯甲烷的提取物有正面效用。當歸的化學成份4-乙基間苯二酚、4-乙基苯酚及1-十四烷醇也能降低小鼠黑色素細胞的黑色素量。數種生化技術繼而被應用作研究有效化學物的藥理。他們包括西方墨點法、環磷酸腺苷測試、蛋白激酶A活性測試及酪氨酸酶活性測試。 / Melanogenesis is a biochemical process designated for protecting skin cells from ultraviolet (UV)-induced damage. During the process, melanin is produced in the melanosomes of the melanocytes located at the basal epidermis of human. The process could be affected by genetic, hormonal or environmental factors. Amount of melanin synthesized depending on the activity of the rate-limiting enzyme tyrosinase, number and size of melanosomes, the transfer rate of melanosomes to keratinocytes through the melanocyte dendritic projections and the distribution pattern of melanosomes within keratinocytes. These cellular processes are influenced by variations in skin color or UV exposure amount. When melanin synthesis exceeds melanin degradation, hyperpigmentation disorder arises. This lead to the formation of freckles or chloasma according to different skin types, age groups and degree of cumulative UV exposure. A number of treatments are commercially available, they include applying synthetic cosmetics, laser, plastic surgery, etc. These treatments usually produce side-effects and possess high risk. Therefore, searching for therapeutic agents from natural compounds has become a new research direction in cosmetology. In this study, ten herbs were chosen from traditional Chinese medicine (TCM) which had been applied for treating hyperpigmentation. The herbs were extracted by four solvents with different polarity. The extracts were screened for their hypopigmentary ability by using melan-a cells. It was found that the hexane and dichloromethane extracts of Angelica sinensis possessed positive effects. 4-ethylresorcinol, 4-ethylphenol and 1-tetradecanol, the chemical constituents of A. sinensis, also attenuated melanin amount in melan-a cells. Moreover, several biochemical techniques were utilized to study the pharmaceutical mechanisms of the potent compounds. They include Western blot, cyclic adenosine monophosphate (cAMP) assay, protein kinase A (PKA) activity assay and tyrosinase activity assay. / Detailed summary in vernacular field only. / Lam, Rosanna Yen Yen. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 127-146). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / Abstract --- p.i / Chinese Abstract --- p.iii / Acknowledgements --- p.iv / List of Publications --- p.v / Table of Contents --- p.vi / List of Abbreviations --- p.xii / List of Figures --- p.xv / List of Tables --- p.xviii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Demand of cosmetics --- p.1 / Chapter 1.2 --- Skin structures and functions --- p.1 / Chapter 1.2.1 --- Epidermis --- p.3 / Chapter 1.2.1.1 --- Stratum corneum --- p.4 / Chapter 1.2.1.2 --- Stratum granulosum --- p.4 / Chapter 1.2.1.3 --- Stratum spinosum --- p.4 / Chapter 1.2.1.4 --- Stratum basale --- p.4 / Chapter 1.2.2 --- Dermis --- p.5 / Chapter 1.2.3 --- Hypodermis --- p.5 / Chapter 1.3 --- Sun irradiation --- p.5 / Chapter 1.4 --- Variety of skin types --- p.6 / Chapter 1.5 --- Biochemical reactions within melanocyte --- p.7 / Chapter 1.6 --- Pigmentation disorder --- p.14 / Chapter 1.7 --- From the view of traditional Chinese medicine --- p.16 / Chapter 1.8 --- Treatments available for hyperpigmentation --- p.18 / Chapter 1.9 --- Aims of study and application of strategies --- p.19 / Chapter Chapter 2 --- Investigation of the inhibitory effect of herbal extracts and their constituent compounds on melanin synthesis --- p.20 / Chapter 2.1 --- Introduction --- p.20 / Chapter 2.2 --- Materials and methods --- p.21 / Chapter 2.2.1 --- Materials --- p.21 / Chapter 2.2.2 --- Herbal extraction --- p.23 / Chapter 2.2.3 --- Cell culture --- p.25 / Chapter 2.2.4 --- Growth curve and melanin production curve --- p.25 / Chapter 2.2.5 --- SRB assay --- p.26 / Chapter 2.2.6 --- Calibration curve for SRB assay --- p.27 / Chapter 2.2.7 --- Measurement of melanin production --- p.27 / Chapter 2.2.8 --- Calibration curve for melanin production assay --- p.28 / Chapter 2.2.9 --- Statistical analysis --- p.28 / Chapter 2.3 --- Results --- p.29 / Chapter 2.3.1 --- Growth curve and melanin production curve for assay development --- p.29 / Chapter 2.3.2 --- Calibration curves of SRB assay and melanin production assay --- p.32 / Chapter 2.3.3 --- Hypopigmentary effect of 40 herbal extracts --- p.35 / Chapter 2.3.4 --- Hypopigmentary effects of chemical components of A. sinensis --- p.41 / Chapter 2.4 --- Discussion --- p.49 / Chapter Chapter 3 --- Study of the effect of potential compounds on melanogenic protein expression by Western blot --- p.54 / Chapter 3.1 --- Introduction --- p.54 / Chapter 3.2 --- Materials and methods --- p.56 / Chapter 3.2.1 --- Materials --- p.56 / Chapter 3.2.2 --- Cell culture --- p.56 / Chapter 3.2.3 --- Preparation of cell lysates --- p.57 / Chapter 3.2.4 --- Protein assay --- p.57 / Chapter 3.2.5 --- SDS-PAGE and membrane transfer --- p.58 / Chapter 3.2.6 --- Washing of blotted antibodies and film exposure --- p.59 / Chapter 3.3 --- Results --- p.61 / Chapter 3.4 --- Discussion --- p.70 / Chapter Chapter 4 --- Study of the effect of potential compounds on melanogenic gene expression by RT-PCR --- p.76 / Chapter 4.1 --- Introduction --- p.76 / Chapter 4.2 --- Materials and methods --- p.76 / Chapter 4.2.1 --- Materials --- p.77 / Chapter 4.2.2 --- Cell culture --- p.77 / Chapter 4.2.3 --- RNA extraction --- p.78 / Chapter 4.2.4 --- cDNA synthesis --- p.78 / Chapter 4.2.5 --- PCR --- p.80 / Chapter 4.3 --- Results --- p.83 / Chapter 4.4 --- Discussion --- p.85 / Chapter Chapter 5 --- Study of the effect of potential compounds on cAMP level by EIA --- p.85 / Chapter 5.1 --- Introduction --- p.86 / Chapter 5.2 --- Materials and methods --- p.86 / Chapter 5.2.1 --- Materials --- p.86 / Chapter 5.2.2 --- Cell culture --- p.86 / Chapter 5.2.3 --- Preparation of cell lysates --- p.86 / Chapter 5.2.4 --- Protein assay --- p.87 / Chapter 5.2.5 --- The cAMP assay --- p.88 / Chapter 5.2.6 --- Preparation of cAMP calibration curve --- p.88 / Chapter 5.2.7 --- Calculation --- p.89 / Chapter 5.2.8 --- Statistical analysis --- p.89 / Chapter 5.3 --- Results --- p.90 / Chapter 5.4 --- Discussion --- p.94 / Chapter Chapter 6 --- Study of the effect of potential compounds on PKA activity by PKA activity assay --- p.96 / Chapter 6.1 --- Introduction --- p.96 / Chapter 6.2 --- Materials and methods --- p.96 / Chapter 6.2.1 --- Materials --- p.97 / Chapter 6.2.2 --- Cell culture --- p.97 / Chapter 6.2.3 --- Preparation of cell lysates --- p.98 / Chapter 6.2.4 --- Protein assay --- p.98 / Chapter 6.2.5 --- The PKA kinase activity assay --- p.100 / Chapter 6.2.6 --- Calculation --- p.100 / Chapter 6.2.7 --- Statistical analysis --- p.100 / Chapter 6.3 --- Results --- p.101 / Chapter 6.4 --- Discussion --- p.104 / Chapter Chapter 7 --- Study of the effect of potential compounds on tyrosinase activity by enzyme inhibition assay --- p.107 / Chapter 7.1 --- Introduction --- p.107 / Chapter 7.2 --- Materials and methods --- p.108 / Chapter 7.2.1 --- Materials --- p.108 / Chapter 7.2.2 --- Assay development for mushroom tyrosinase --- p.109 / Chapter 7.2.3 --- Mushroom tyrosinase inhibition assay --- p.109 / Chapter 7.2.4 --- Cell culture --- p.110 / Chapter 7.2.5 --- Preparation of cellular tyrosinase --- p.110 / Chapter 7.2.6 --- Protein assay --- p.111 / Chapter 7.2.7 --- Cellular tyrosinase inhibition assay --- p.111 / Chapter 7.2.8 --- Calculation --- p.112 / Chapter 7.2.9 --- Statistical analysis --- p.112 / Chapter 7.3 --- Results --- p.113 / Chapter 7.4 --- Discussion --- p.120 / Chapter Chapter 8 --- General discussion --- p.123 / References --- p.127

In a mouse model of pulmonary thromboembolism induced by a collagen-adrenaline mixture, the SFE extract and ligustilide reduced the paralysis-death ratio, and the anti-thrombotic response of senkyunolide A was more pronounced. The effect of BDPH was not significant. Neither the SFE extract nor the three phthalides prolonged bleeding time in tail-transected mice. / In a rat myocardial ischemia-reperfusion model involving coronary artery ligation, 7-day pre-treatment with the SFE extract and ligustilide reduced ventricular arrhythmias in isolated hearts. BDPH and senkyunolide A were without significant effects. / In rat platelet-rich plasma, platelet aggregation induced by collagen and U46619 but not by adenosine diphosphate was inhibited by the SFE extract. Ligustilide inhibited the responses of all three agonists, while BDPH and senkyunolide A inhibited the collagen response only. / Raw Rhizoma Chuanxiong herb and its crude extract as obtained by supercritical fluid extraction (SFE) comprised mainly phthalides. The SFE extract and three representative phthalides, butylidenephthalide (BDPH), ligustilide and senkyunolide A, were studied on vasorelaxation, myocardial ischemia, platelet aggregation and thrombosis. The mechanisms underlying BDPH-mediated vasorelaxation were also explored. / Rhizoma Chuanxiong, the dried rhizome of Ligusticum chuanxiong Hort., is a common traditional Chinese medicine used for the treatment of cardiovascular diseases. Surprisingly, the scientific basis of its action is poorly understood. The current study aims to establish the pharmacological basis of the cardiovascular effects of Rhizoma Chuanxiong and its active constituents by examining their effects in several cardiovascular domains. / The current study demonstrated various cardiovascular actions of Rhizoma Chuanxiong, and thereby established the pharmacological basis of the effects of the herb. Phthalides, in particular BDPH, ligustilide and senkyunolide A, were important contributors to such actions. Future investigation of the SFE extract and/or individual phthalides related to the progression from in vitro and in vivo effectiveness to clinical efficacy is much anticipated. / The SFE extract, BDPH, ligustilide and senkyunolide A produced vasorelaxation on isolated preparations of rat aorta, rat saphenous vein and pig coronary artery. BDPH-mediated relaxation appeared to involve both extracellular Ca 2+-dependent (L-type voltage-operated, receptor-operated and store-operated Ca2+ channels) and independent (NO modulation, Ca2+ release from internal stores and Ca2+ desensitization) mechanisms. BDPH was also observed to augment relaxation induced by sodium nitroprusside and forskolin through mechanisms that remain undefined. / Chan Sun Kin Sunny. / "July 2005." / Advisers: G. Lin; R. L. Jones. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1575. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 190-209). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Chan Chun-pong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 171-176). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / 摘要 --- p.iii / Abbreviation --- p.iv / Table of contents --- p.v / List of figures --- p.xi / List of tables --- p.xvi / Chapter Chapter 1 --- introduction / Chapter 1.1 --- Traditional Chinese medicines (TCMs) --- p.2 / Chapter 1.2 --- Liver disorders in Asia Pacific region --- p.3 / Chapter 1.3 --- Classification of liver disorders --- p.7 / Chapter 1.3.1 --- Hepatitis --- p.8 / Chapter 1.3.1.1 --- Hepatitis A virus infection --- p.8 / Chapter 1.3.1.2 --- Hepatitis B virus infection --- p.9 / Chapter 1.3.1.3 --- Hepatitis C virus infection --- p.11 / Chapter 1.3.1.4 --- Hepatitis D virus infection --- p.12 / Chapter 1.3.1.5 --- Hepatitis E virus infection --- p.12 / Chapter 1.3.2 --- Cancer of the liver --- p.13 / Chapter 1.3.2.1 --- Hepatocellular carcinoma --- p.13 / Chapter 1.3.2.2 --- Cholangiocarcinoma --- p.14 / Chapter 1.3.2.3 --- Metastatic liver cancer --- p.14 / Chapter 1.4 --- Conventional treatment of liver disorders --- p.14 / Chapter 1.5 --- Role of traditional Chinese medicines in hepatoprotective functions --- p.16 / Chapter 1.5.1 --- Abri Herba (Abrus Cantoniensis Hance) --- p.17 / Chapter 1.5.2 --- Rhizoma Coptidis (Coptidis chinensis Franch) --- p.18 / Chapter 1.5.3 --- Fructus Forsythia (Forsythia suspense (Thunb) Vahl) --- p.22 / Chapter 1.6 --- Molecular studies of hepatoprotective effects of TCMs --- p.26 / Chapter 1.6.1 --- Roles of detoxofication enzymes in hepatoprotection --- p.27 / Chapter 1.6.2 --- Studies of growth-related genes in cell cycle control --- p.29 / Chapter 1.7 --- Aims of project --- p.32 / Chapter 1.8 --- Application of the project --- p.33 / Chapter Chapter 2 --- Methods and materials --- p.34 / Chapter 2.1 --- Screening of traditional Chinese medicines --- p.35 / Chapter 2.2 --- Preparation of TCMs --- p.35 / Chapter 2.2.1 --- Preparation of aqueous extracts of TCMs --- p.35 / Chapter 2.2.2 --- Preparation of active components of TCMs --- p.36 / Chapter 2.3 --- In vitro assays --- p.40 / Chapter 2.3.1 --- Cell culture --- p.40 / Chapter 2.3.2 --- Cytotoxicity test --- p.40 / Chapter 2.4 --- Screening of expressed gene induced by TCMs --- p.41 / Chapter 2.4.1 --- RNA preparation --- p.41 / Chapter 2.4.2 --- cDNA array hybridization --- p.42 / Chapter 2.4.3 --- Reverse Transcription --- p.43 / Chapter 2.5 --- Confirmation of expressed genes induced by TCMs --- p.44 / Chapter 2.5.1 --- Semi-quantitative PCR analysis --- p.44 / Chapter 2.5.2 --- Northern blot analysis --- p.46 / Chapter 2.6 --- Studies of effects of TCMs in gene expression --- p.47 / Chapter 2.6.1 --- Dosage-course study --- p.47 / Chapter 2.6.2 --- Time-course study --- p.48 / Chapter Chapter 3 --- Results --- p.50 / Chapter 3.1 --- "Cytotoxicity test of A.H., R.C. and F.F" --- p.51 / Chapter 3.2 --- "Molecular screening of expressed gene induced by A.H., R.C., F.F" --- p.58 / Chapter 3.3 --- Confirmation of expressed gene using semi-quantitative RT- PCR --- p.70 / Chapter 3.3.1 --- Dosage-course and time-course studies of A.H. using RT- PCR --- p.70 / Chapter 3.3.2 --- Dosage-course and time-course studies of R.C. using RT- PCR --- p.94 / Chapter 3.3.3 --- Dosage-course and time-course studies of A.H. using RT- PCR --- p.113 / Chapter 3.4 --- Confirmation of expressed gene using northern blot anaylsis --- p.118 / Chapter 3.4.1 --- Dosage-course and time-course studies of effects of A.H. and L- abrine in Northern blot analysis --- p.118 / Chapter 3.4.2 --- Dosage-course and time-course studies of effects of R.C. and berberine in Northern blot analysis --- p.129 / Chapter 3.4.3 --- Dosage-course and time-course studies of effects of F.Fin Northern blot analysis --- p.147 / Chapter Chapter 4 --- Discussion --- p.152 / Chapter 4.1 --- "Roles of A.H., R.C. and F.F. in treatment and prevention of liver disorders" --- p.153 / Chapter 4.2 --- "Cytotoxicity effect A.H., R.C., and F.F. in liver cells" --- p.153 / Chapter 4.3 --- Effects of herbal medicines on the transcription of mRNA in liver cells --- p.155 / Chapter 4.3.1 --- Effects of treatment of A.H. in liver at transcriptional level … --- p.155 / Chapter 4.3.2 --- Effects of treatment of R.C. in liver at transcriptional level … --- p.156 / Chapter 4.3.3 --- Effects of treatment of R.C. in liver at transcriptional level --- p.157 / Chapter 4.4 --- Comparison of results of RT-PCR and Northern blot analysis --- p.157 / Chapter 4.4.1 --- Comparison of the effects of time and dosage-course studies of DTD expression induced by A.H. and L-abrine --- p.157 / Chapter 4.4.2 --- Comparison of the effects of time and dosage-course studies of p21;cip;waf1 expression induced by A.H. and L-abrine --- p.158 / Chapter 4.4.3 --- Comparison of the effects of time and dosage-course studies of c-myc responsive protein; rcl expression induced by R.C. and berberine --- p.159 / Chapter 4.4.4 --- Comparison of the effects of time and dosage-course studies of GST Ya expression induced by R.C. and berberine --- p.160 / Chapter 4.4.5 --- Comparison of the effects of time and dosage-course studies of GST 7-7 expression induced by F.F --- p.160 / Chapter 4.5 --- Biochemical significance of genes induced by hepatoprotective TCMs --- p.161 / Chapter 4.5.1 --- Roles of significant expression of detoxifying enzymes induced by TCMs in liver cells --- p.161 / Chapter 4.5.2 --- Roles of induction of growth-related c-myc responsive protein; rcl in R.C. treated liver cells --- p.167 / Chapter 4.5.3 --- Roles of increased p21;cip;waf1 expression in A.H. treated liver cells --- p.168 / Chapter 4.6 --- Conclusion --- p.169